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Objective: To observe the effects of panaxtriol saponin (PTS) on CK-MB, cTnI, IL-6, TNF-α, and ultrastructure against myocardial ischemia-reperfusion injury (MIRI) in rats. Methods: Wistar rats were randomly divided into six groups: Sham, MIRI model, positive control, and 22.5, 45, and 90 mg/kg PTS groups. Animal MIRI model was made by ligating the left anterior descending coronary artery. Drug was given for seven consecutive days before the operation by ip injection. Rats were sacrificed after 30 min ischemia and 24 h reperfusion. CK-MB, cTnI, IL-6, and TNF-α in serum were measured and the changes of myocardial ultrastructure were observed. Real time PCR was used to evaluate change of NRF2 and HO-1 mRNA level in myocardial tissue. Results: Compared with model, PTS 45 and 90 mg/kg reduced the CK-MB, cTnI, IL-6, and TNF-α in serum and improve the myocardium ultrastructure. Nrf2 and HO-1 mRNA levels in PTS treatment group were higher than those in MIRI model group. Conclusion: PTS plays a crucial role in cardioprotection against the ischemia and reperfusion injury in rats. The protective mechanism suggests that PTS could stimulate NRF2/HO-1 expression in myocardial tissue and then inhibit myocardial inflammation.
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ObjectiveToinvestigatetherolesofbrain-derivedneurotrophicfactor(BDNF)and tyrosine receptor kinase B (TrkB) in ischemic postconditioning. Methods Wistar rats w ere randomly assigned to three groups:a sham operation (9 rats), an ischemic postconditioning, and an ischemia-reperfusion group. According to the reperfusion time, the latter 2 groups w ere redivided into 6, 12, 24, 48, and 72 h subgroups (9 rats in each subgroups). A middle cerebral artery occluded by suture method for a cerebral ischemia-reperfusion model. Triphenyl tetrazolium staining w as used to detect infarct volume (P=4). Immunohisto-chemical staining w as used to detect the expression levels of BDNF and TrkB proteins (P=5). Results The infarct volumes in the ischemic postconditioning group w ere reduced significantly compared w ith those in the ischemia-reperfusion group (6 h:143.3 ±8.7 mm3 vs.166.8 ±7.5 mm3, t=4.104, P=0.006;12 h:151.7 ±7.8 mm3 vs.171.6 ±9.1 mm3, t=3.314, P=0.016; 24 h: 159.2 ±9.3 mm3 vs.177.1 ± 7.6 mm3, t=3.000, P=0.024;48 h:166.9 ±9.6 mm3 vs.184.9 ±9.0 mm3, t=2.732, P=0.034;72 h:172.0 ±9.1 mm3 vs.198.1 ±8.2 mm3, t=2.640, P=0.039), and the positive cel numbers of BDNF (6 h:23.98 ±4.07 vs.18.63 ±2.5, t=2.479, P=0.038;12 h:27.64 ±3.18 vs.22.01 ±3.14, t=2.817, P=0.023;24 h:34.82 ±4.17 vs.28.46 ±4.05, t=2.446, P=0.040; 48 h:34.30 ±3.27 vs.26.29 ± 3.26, t=3.872, P=0.005;72 h:28.77 ±3.53 vs.23.64 ±3.54, t=2.297, P=0.051) and TrkB (6 h:33.83 ±3.90 vs.21.51 ±3.86, t=5.012, P<0.001; 12 h:38.59 ±4.84 vs.23.41 ±3.67, t=5.586, P<0.001;24 h:46.07 ±3.06 vs.28.78 ±3.61, t=8.169, P<0.001; 48 h:47.90 ±3.30 vs.29.51 ± 3.81, t=8.160, P<0.001; 72 h:42.78 ±4.07 vs.27.46 ±3.19, t=6.623, P<0.001) per high-pow er field at each time point in the ischemic postconditioning group w ere significantly more than those in the ischemia-reperfusion group. Conclusions Ischemic postconditioning upregulates the expressions levels of BDNF and TrkB proteins after ischemia-reperfusion and reduces cerebral infarct volumes. BDNF/TrkB may play an important neuroprotective effect in ischemic postconditioning.
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ObjectiveTo investigate the protective effect of sevoflurane postconditioning (Sevo-Postcon)on the hearts isolated from rats with diabetes mellitus (DM) of different duration against ischemia-reperfusion (I/R)injury.MethodsSeventy-two pathogen-free male SD rats weighing 200-240 g were randomly divided into 3 groups ( n =24 each):group Ⅰ rats without DM (C) ; group Ⅱ rats with 2 week DM (2w DM) and group Ⅲ rats with 6 week DM (6w DM).DM was produced by intraperitoneal (IP) 1％ streptozocin (STZ) 60 mg/kg and confirmed by fasting blood glucose concentration ＞ 16.7 mmol/L in groups Ⅱ and Ⅲ.Hearts were isolated from rats and perfused with Krebs-Henseleit buffer (KHB) in a Langendorff apparatus.After a 15 min stabilization period,the isolated hearts were subjected to 30 min of global no-flow ischemia followed by 75 min of reperfusion.Twelve hearts in each group were perfused after ischemia with KHB saturated with 3％ Sevo for 15 min followed by perfusion with regular KHB for 60 min.LVEDP,LVDP, ± dp/dt and HR were measured and recorded after 15 min stabilization (T0,baseline) and at 15 and 75 min of reperfusion (T1,2 ).Myocardial specimens were obtained at 15 min of reperfusion (T1) for detection of p-Akt expression (by Western blot analysis).Infarct size was determined at 75 min of reperfusion (T2).ResultsSevo-Postcon significantly improved cardiac function,reduced infarct size and up-regulated p-Akt expression in groups Ⅰ (C) and Ⅱ (2w DM),while in group Ⅲ (6w DM) Sevo-Postcon did not cause any change in cardiac function,infarct size and p-Akt expression as compared with the isolated hearts without Sevo-Postcon.ConclusionThe cardioprotective effect of Sevo-Postcon can be attenuated with increasing duration of DM by impairing PI3K/Akt signaling pathway.
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Objective To observe the neuron apoptosis and anti-oxidative stress function of cerebral tissues after acute cerebral ischemia/reperfusion (I/R) in rats treated with apelin in the early period of acute cerebral I/R. Methods Totally 156 male Wistar rats were randomly divided into 3 groups: sham group (n=12), ischemia reperfusion group (I/R group, n=72) and ischemia reperfusion plus apelin group (I/R+AP group, n=72). The latter two groups were further divided into 6 subgroups according to reperfusion time (3, 6, 12, 24, 72, and 120 h groups, each group containing 12 rats). Apelin (10-7 mol/L \[10 μl\]) was injected into the lateral ventricle in the early time of reperfusion (30 min) in the I/R+AP group. RT-PCR was used to observe the change of caspase-3 and caspase-12 mRNA expression in the injured side of cerebral cortex in each group, and flow cytometer was employed to detect the apoptosis rate of neurons. The content of malondialdehyde (MDA), activity of glutathione peroxidase (GSH-Px), and the total antioxidant capacity were also examined in the brain homogenate after I/R. Results The expression of caspase-3 mRNA and caspase-12 mRNA was increased in I/R and I/R+AP groups compared with the sham group. Treatment with apelin down-regulated caspase-12 mRNA expression but had little influence on caspase-3 mRNA expression. The neuron apoptosis rate was significantly lower in I/R+AP group compared with the I/R group (P<0.05), and the changes increased with time. Compared with the sham group, I/R group had significantly increased MDA content(P<0.05) and significantly decreased GSH-Px activity and total antioxidant capacity (P<0.05). Compared with the I/R group, I/R+AP group had significantly increased GSH-Px activity and total antioxidant capacity and significantly decreased MDA content (P<0.05). Conclusion Early intervention with apelin can protect the neurons in rats after acute cerebral I/R.
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Objective To study the effects of DMPS on IL-1? during experimental myocardial ischemia-reperfusion(I/R)injury.Methods 30 New Zealand rabbits were randomly assigned to 3 groups:I/R group,DMPS protection group and Control group,10 in each group.The blood samples was obtained through vien at different time(5 min before ischemia,the end of the ischemia period and 0.5h,1h,2h,4h,6h after reperfusion)in each group.The serum concentrations of IL-1? were detected with radioimmunology method.Cardiac tissues samples were taken for determination of IL-1?.The ultrastructure changes of the Cardiac tissues were observed.Results The levels of IL-1? of serum and cardiac tissues increased after ischemia and reperfusion,and were significant different comparing with that before ischemia(P
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Objective To study the potential role of tumor necrosis factor-α (TNF-α) induction in the development of mucosal barrier dysfunction in rats caused by acute intestinal ischemia-reperfusion injury, and to examine whether pretreatment with monoclonal antibody against TNF-α (TNF-α MoAb) would affect the release of D(-)-lactate after local gut ischemia followed by reperfusion. Methods Anesthetized Sprague-Dawley rats underwent superior mesenteric artery occlusion for 75 min followed by reperfusion for 6 hr. The rats were treated intravenously with either TNF-α MoAb (20 mg/kg) or albumin (20 mg/kg) 30 min prior to the onset of ischemia. Plasma D(-)-lactate levels were measured in both the portal and systemic blood by an enzymatic spectrophotometric assay. Intestinal TNF-αmRNA expression as well as protein levels were also measured at various intervals. In addition, a postmortem examination was performed together with a macropathological evaluation based on a four-grade scoring system.Results Intestinal ischemia resulted in a significant elevation in D(-)-lactate levels in the portal vein blood in both the control and treatment groups ( P ＜0.05). However, animals pretreated with TNF-α MoAb at 6 hr after reperfusion showed significant attenuation of an increase in both portal and systemic D(-)-lactate levels when compared with those only receiving albumin (P ＜ 0.05). In the control animals, a remarkable rise in intestinal TNF-α level was measured at 0.5 hr after clamp release ( P ＜ 0.01); however, prophylactic treatment with TNF-α MoAb completely annulled the increase of local TNF-α levels seen in the control animals. Similarly, after anti-TNF-α MoAb administration, intestinal TNF-α mRNA expression was markedly inhibited, which showed significant differences when compared with the control group at 0.5 hr, 2 hr and 6 hr after the release of occlusion ( P ＜ 0.05-0.01 ). In addition, the pathological examination showed marked intestinal lesions that formed during ischemia, which were much worse upon reperfusion,particularly at the 6 hr time point. These acute injuries were obviously attenuated in animals receiving TNF-α MoAb.Conclusions It appeared that acute intestinal ischemia was associated with failure of the mucosal barrier, resulting in increased plasma D(-)-lactate levels in both portal and systemic blood. These results suggest that TNF-α appears to be involved in the development of local damage associated with intestinal ischemic injury. Moreover, prophylactic treatment with TNF-α MoAb exerts preventive effects on ischemia/ reperfusion-induced circulating D (-)-lactate elevation and gut injury. ( J Geriatr Cardiol 2004;1(2):119-124. )
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Objective: To explore the myocardial protection of induction and reperfusion with warm blood cardioplegia for hypoxic immature myocardium. Methods: A hypoxic model of neonatal rabbits was established in this study. Some indexes,such as myocardial energy metabolism, water content, SOD, MDA and myocardial ultrastucture, were observed after induction and reperfusion with warm blood cardioplegia, comparing to cold crystalloid cardioplegia. Results: Hypoxic neonatal rabbits in this study presented cyanotis, hypoxemia and higher ratio of RV/(LV+S) simulating the pathophysiological changes in cyanotic congenital heart disease. It could be built and repeated easily in experimental researches of immature myocardial protection. Myocardial ATP content was (13.09?1.50) ?mol/g in studying group versus (11.53?5.40)?mol/g in control group (P
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The effects of propylene glycol mannate sulfate (PGMS) on the lipid peroxide (MDA) , superoxide dismutase (SOD) , glutathion peroxidase (GSH-Px), nitric oxide (NO)and water content in the whole cerebral ischemia/reperfusion injury rabbits induced by four-vessel occlusion,The results show that PGMS can decrease the brain water and MDA, and can increase the SOD and GSH-Px level. No significant effect on the NO level has been detected. The results suggest that the protective effects of PGMS on ischemia/reperfusion injury may be related to its antioxidation.